ObjectiveCerebral venous sinus thrombosis (CVST) is a rare cerebrovascular disease affecting young adults. The majority of the patients are female. The aim of this study is to assess the clinical associations, risk factors and outcomes of the patients with CVST.MethodsThe data of 75 patients with CVST admitted to our hospital between 2006 and 2016 were reviewed. Demographic and clinical features and the thrombophilic risk factors of the patients were recorded. The localizations of the thrombi were determined and modified Rankin score at the time of onset and discharge were calculated.ResultsThe majority of our patients (78.7%) were female. Median age was 35 years (16–76). The most common symptom was headache (86.7%). In 82.6% of our patients, inherited or acquired risk factors for thrombosis were detected. Transverse sinus was the most common site of thrombosis followed by sigmoid and superior sagittal sinuses. Two thirds of the patients had involvement of multiple sinuses. The patients with the involvement of sagittal sinus had better disability at the time of admittance (p = 0.013) while the number of involved sinuses was correlated worse disability (p = 0.015). The neurologic states in the majority of the patients were improved by the end of the hospitalization period (p = 0.001). There was no significant difference in disability score at discharge between men and women (p = 0.080). No patient with CVST died in the hospitalization period.ConclusionsThis study is one of the largest cohort studies on CVST in our region. The results of the study disclosed that CVST had wide range of clinical manifestations and non-specific symptoms at the beginning. For that reason, in especially high risk groups for thrombosis, the diagnosis of CVST should be kept in mind.

It has been hypothesized that chronic inflammation may play an important role in the development and progression of the neurodegeneration of Idiopathic Parkinson's disease (IPD). Neutrophil-lymphocyte ratio (NLR) is a marker that indicates the peripheral inflammation. There is only one study regarding NLR and IPD. In this study, we assessed to investigate NLR in patients with IPD, comparing the results with controls and to determine whether there is a difference in NLR levels in subgroups of IPD (akinetic-rigid and tremor-dominant) differ in their levels of NLR. Medical records of 200 IPD patients and 60 controls reviewed retrospectively. Forty-six IPD patients met the inclusion criteria. NLR was calculated by dividing neutrophil count to lymphocyte count. Thirteen akinetic-rigid (AR-IPD) and thirty-three tremor-dominant (TD-IPD) patients' and controls results were compared. There was not a statistically difference between the NLR levels of IPD patients, controls, and AR-IPD and TD-IPD patients. This result suggests that cerebral inflammation is in the forefront in the development of neurodegeneration in IPD, and that more evidence is needed for the role of peripheral inflammation in the development progression of disease.

Parkinson's disease (PD) is one of the common neurodegenerative disorders. Oxidative stress is considered as a contributing factor to the development of PD. The present study aims to investigate serum oxidative stress status in patients with PD. Oxidative stress was assessed by measuring serum nitric oxide levels, lipid hydroperoxide concentrations, and nitric oxide synthase activity. In addition, total serum antioxidant capacity (TAC) was evaluated using the serum 2,2-Diphenyl-1-picryl-hydrazyl (DPPH) free-radical scavenging method in 32 patient with Parkinson's disease and 32 control subjects. Our results indicated that serum nitric oxide and lipid hydroperoxide levels were significantly lower in patients with PD than controls. Moreover, nitric oxide levels were found to be negatively correlated with Unified Parkinson's Disease Rating Scale (UPDRS). However, no statistical difference was observed in total serum antioxidant capacities and nitric oxide synthase activities between patients and controls. The present study indicates that although antioxidant capacity was not changed, lipid hydroperoxide (LPO) level was found decreased. This might show pre-oxidative process in these patients. In addition, decreased nitric oxide (NO) level and negative correlation observed between NO level and disease rating scale implicated a role for NO in the disease process.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Oxidative stress has been hypothesized to play a major role in the development of PD in various studies. This study assessed to investigate oxidative and anti-oxidative status in PD patients. We evaluated oxidant/antioxidant status by measuring serum malondialdehyde (MDA) levels, xanthine oxidase (XO) activities, and activities of antioxidant enzymes, namely, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). The study included 29 patients with PD and 32 healthy subjects as controls. Comparison of oxidative parameters in the patient and control groups revealed significantly higher GSH-Px and XO activities in the patient group. Serum MDA and SOD activities in PD patients were not significantly different from the controls. MDA was negatively correlated with duration of the PD and positively with age of onset. There was a negative correlation between SOD and Hoehn and Yahr (H&Y) stage. According to these results, we suggest that oxidative stress may contribute to the development of PD.

Oxidative stress has been implicated in various disorders, including epilepsy. The aim of this study was to investigate the oxidant and antioxidant status of patients with epilepsy using antiepileptic drugs regularly and to compare them with healthy subjects. We investigated serum catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and xanthine oxidase (XO) levels in 58 epilepsy patients and 25 healthy controls. Patients were divided into polytherapy (n = 17) and monotherapy (n = 41) groups, and antioxidant status was compared between the two groups and controls. There was no significant difference between the patient and control groups in terms of age or gender (p > 0.05). The mean duration of illness in the patients was 14.8 years, and the mean duration of treatment was 11.4 years. Comparison of the patient and control groups in terms of oxidative stress and antioxidant defence parameters revealed significantly higher MDA, GSH-Px, XO and lower level of CAT, SOD levels (p < 0.05). There were no differences in CAT, MDA, GSH-Px or SOD levels between the monotherapy and polytherapy groups; but the XO level was higher in the monotherapy group (p < 0.05). Although the XO level was decreased by polytherapy, it was higher than in controls. Our study found significantly low level of antioxidants in patients with epilepsy as compared to control. Thus, antiepileptic treatment did not improve oxidative stress parameters. Furthermore, our results show that polytherapy does not change the situation as compared with monotherapy. Antioxidant replacement therapy may benefit these patients.